Anemia of Prematurity - Portal Neonatal

Deterrence/Prevention:
• The multifactorial etiology of BPD compounds its prevention.
• Prenatal steroid therapy and postnatal surfactant use has improved survival and perhaps
redirected severity of BPD.
• Postnatal corticosteroid use may facilitate ventilator weaning but is fraught with many adverse
effects. Reconsider standard of care therapy with postnatal dexamethasone, weighing the
risk-to-benefit ratio in each case.
• Use of exogenous surfactant has improved neonatal survival but may increase the prevalence
of BPD in preterm infants.
• Meticulous attention to oxygen and PPV may modify BPD.
• Maximizing nutritional support, careful monitoring of fluid intake, and judicious diuretic use
helps promote lung healing.
• Conclusive evidence of HFV use to prevent BPD is not currently available.
• Inhaled NO may improve oxygenation in some infants with BPD, but synergistic toxicity of
hyperoxia and NO on pulmonary and surfactant systems has been demonstrated in vitro.
• Davis in 2000 and Rosenfeld et al in 1986 completed human studies of recombinant SOD
supplementation to prevent BPD in preterm infants. In preliminary studies, prophylactic use of
recombinant SOD revealed that it is safe and may modify disease severity. Results of the
most recent phase III efficacy trial are soon to be forthcoming. Effective prevention of BPD has
yet to be found.
Complications:
• Chorioamnionitis, PVL, severe intraventricular hemorrhage, ventriculomegaly, sepsis, and
severe retinopathy of prematurity all are important confounding variables that can greatly
affect infant outcome.
Prognosis:
• Most neonates with BPD ultimately survive; however, these infants are at increased risk for
serious infections, airway hyperreactivity, cardiac dysfunction, and neurologic impairments.
o Since the routine use of surfactant replacement has begun, survival of the most immature
infants has improved. Along with other advances in technology and improved
understanding of neonatal physiology, infants with BPD today appear to have less disease
severity as compared to infants in years past. Infants with severe BPD remain at high risk
for pulmonary morbidity and mortality during the first 2 years of life.
o Fortunately, pulmonary function slowly improves in most survivors with BPD, likely
secondary to continued lung and airway growth and healing. Northway followed the cases
of patients with BPD to adulthood. Northway reported in 1992, that these patients had
airway hyperreactivity, abnormal pulmonary function, and hyperinflation noted on chest
radiography. Rehospitalization for impaired pulmonary function is most common during
the first 2 years of life. In 1990, Hakulinen et al found a gradual decrease in symptom
frequency in children aged 6-9 years as compared to the first 2 years of life. Bader in 1987
and Blayney et al in 1991 found persistence of respiratory symptoms and abnormal PFT
results in children aged 7 and 10 years, respectively. High-resolution chest CT scanning
or MRI studies in children and adults with a history of BPD reveal lung abnormalities that
correlate directly with the degree of pulmonary function abnormality. Postsurfactant
studies of infants with BPD have yielded similar results of improved pulmonary function
with time. Northway reported cor pulmonale in 36% of survivors. Oxygen supplementation
at home is not infrequently required, and failure to relieve pulmonary hypertension with
oxygen may be associated with a poor prognosis.
o Persistent right ventricular hypertrophy or fixed pulmonary hypertension unresponsive to
oxygen supplementation on cardiac catheterization portends a poor prognosis.